作者: Jeffrey S Mogil , Susan P Richards , Laurie A OʼToole , Melinda L Helms , Steve R Mitchell
DOI: 10.1016/S0304-3959(97)03333-2
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摘要: The inbred mouse strains, DBA/2J (D2) and C57BL/6J (B6), display differential sensitivity to acute, thermal nociception as measured on the hot-plate (HP) assay. In an ongoing quantitative trait locus (QTL) mapping study designed reveal genomic loci showing genetic linkage HP sensitivity, a putative QTL chromosome 4 (50–80 cM from centromere) has been identified that appears account for variability in this male, but not female mice. An obvious candidate gene located same chromosomal region is Oprd1, which encodes murine δ-opioid receptor. attempt evaluate whether Oprd1 represents sex-specific we tested D2 B6 mice of both sexes latencies (hindpaw-lift, -lick or -flutter) following systemic injections saline, opioid receptor antagonists naloxone (NAL; 0.1 10 mg/kg), nor-binaltorphimine (nor-BNI; 5 naltrindole (NTI; 7-benzylidenenaltrexone (BNTX; 0.7 naltriben (NTB; 1 mg/kg). High-dose (10 mg/kg) NAL lowered D2, mice, suggesting higher exhibited by reflect mechanisms. strains were unaffected pretreatment with low-dose (0.1 nor-BNI, neither μ nor κ receptors affect basal nociceptive sensitivity. δ-receptor antagonist, NTI, δ2-specific NTB, (but δ1-specific BNTX) effectively strain- sex-dependent manner: male>B6 male>D2 female>B6 female. These data support possibility mediating more generally illustrate important roles background gender perception pain.